Evidence map›Paper›PMID 26512655›Full record

ArticleInternational journal of molecular sciences2015

TP53inp1 Gene Is Implicated in Early Radiation Response in Human Fibroblast Cells.

Nikolett Sándor, Boglárka Schilling-Tóth, Enikő Kis, Lili Fodor, Fruzsina Mucsányi, Géza Sáfrány, Hargita Hegyesi

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Nikolett SándorDivision of Molecular Radiobiology, National Public Health Center-National Research Directorate for Radiobiology and Radiohygiene, Anna 5, Budapest 1221, Hungary. sandor.nikolett@osski.hu.
Boglárka Schilling-TóthDivision of Molecular Radiobiology, National Public Health Center-National Research Directorate for Radiobiology and Radiohygiene, Anna 5, Budapest 1221, Hungary. schilling.toth.boglarka@osski.hu.
Enikő KisDivision of Molecular Radiobiology, National Public Health Center-National Research Directorate for Radiobiology and Radiohygiene, Anna 5, Budapest 1221, Hungary. kis.eniko@osski.hu.
Lili FodorDepartment of Genetics, Cell and Immunobiology, Semmelweis University, Nagyvárad tér 4, Budapest 1089, Hungary. fodorlilierika@gmail.com.
Fruzsina MucsányiDepartment of Genetics, Cell and Immunobiology, Semmelweis University, Nagyvárad tér 4, Budapest 1089, Hungary. fruzsimu@gmail.com.
Géza SáfrányDivision of Molecular Radiobiology, National Public Health Center-National Research Directorate for Radiobiology and Radiohygiene, Anna 5, Budapest 1221, Hungary. safrany.geza@osski.hu.
Hargita HegyesiDivision of Molecular Radiobiology, National Public Health Center-National Research Directorate for Radiobiology and Radiohygiene, Anna 5, Budapest 1221, Hungary. hegyesi.hargita@osski.hu.
Semmelweis University · HUFrédéric Joliot-Curie National Research Institute for Radiobiology and Radiohygiene · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor protein 53-induced nuclear protein-1 (TP53inp1) is expressed by activation via p53 and p73. The purpose of our study was to investigate the role of TP53inp1 in response of fibroblasts to ionizing radiation. γ-Ray radiation dose-dependently induces the expression of TP53inp1 in human immortalized fibroblast (F11hT) cells. Stable silencing of TP53inp1 was done via lentiviral transfection of shRNA in F11hT cells. After irradiation the clonogenic survival of TP53inp1 knockdown (F11hT-shTP) cells was compared to cells transfected with non-targeting (NT) shRNA. Radiation-induced senescence was measured by SA-β-Gal staining and autophagy was detected by Acridine Orange dye and microtubule-associated protein-1 light chain 3 (LC3B) immunostaining. The expression of TP53inp1, GDF-15, and CDKN1A and alterations in radiation induced mitochondrial DNA deletions were evaluated by qPCR. TP53inp1 was required for radiation (IR) induced maximal elevation of CDKN1A and GDF-15 expressions. Mitochondrial DNA deletions were increased and autophagy was deregulated following irradiation in the absence of TP53inp1. Finally, we showed that silencing of TP53inp1 enhances the radiation sensitivity of fibroblast cells. These data suggest functional roles for TP53inp1 in radiation-induced autophagy and survival. Taken together, we suppose that silencing of TP53inp1 leads radiation induced autophagy impairment and induces accumulation of damaged mitochondria in primary human fibroblasts.

Indexed as

AutophagyCarrier ProteinsCell LineCellular SenescenceCyclin-Dependent Kinase Inhibitor p21DNA, MitochondrialFibroblastsGrowth Differentiation Factor 15Heat-Shock ProteinsHumansCarrier ProteinsCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21DNA, MitochondrialGDF15 protein, humanGrowth Differentiation Factor 15Heat-Shock ProteinsTP53INP1 protein, humanautophagyCDKN1AGDF-15p53-networkradiosensitivityRNA interferencesenescenceTP53inp1

Identifiers

PMID26512655
PMCPMC4632809
OpenAlexW1859709850

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.